MSN 671 Final UPDATED ACTUAL QUESTIONS AND CORRECT
Answers
Classic synaptic neurotransmission Action potential traveling down the presynaptic axon. Upon reaching the terminal
Ca²⁺ enters through voltage-sensitive calcium channels, triggering the exocytosis
of neurotransmitter-filled vesicles into the synaptic cleft. The released
neurotransmitters (e.g., dopamine, serotonin, norepinephrine) then bind to
postsynaptic receptors, initiating a new electrical signal in the receiving neuron.
Ligand-gated ion channel open upon neurotransmitter binding to allow rapid ion passage
Voltage-sensitive ion channel open in response to electrical changes to propagate action potentials.
Sodium-charged ion channel type of voltage-sensitive channel essential for depolarization
Presynaptic transporter (DAT, SERT, NET) clear neurotransmitters from the cleft to end the signal
Norepinephrine (NE) Regulates attention and arousal; low levels may result in ADHD/depression, while
high levels can lead to anxiety
Acetylcholine Crucial for memory and learning; deficiency is linked to Alzheimer's disease,
whereas excess may cause muscle cramps/seizures
Melatonin Synthesized in the pineal gland during darkness, it regulates the circadian rhythm
and promotes sleep
, Serotonin Modulates mood and appetite; its deficiency can cause depression/anxiety, and
excess may trigger serotonin syndrome
Dopamine Key for reward and motor control; deficiency is associated with Parkinson's and
depression, while excess is linked to schizophrenia
GABA Provides inhibitory control to prevent neuronal overexcitation; low levels may
lead to anxiety and seizures, high levels to sedation
Histamine Maintains wakefulness; overactivity can cause insomnia, and blockade (by some
antipsychotics) results in sedation and weight gain
Process of melatonin production During darkness, the pineal gland synthesizes melatonin from serotonin using N-
acetyltransferase. Melatonin levels rise at night, signaling sleep onset by acting on
MT1/MT2 receptors to regulate the circadian rhythm
Causes Tardive Dyskinesia with an antipsychotic Tardive dyskinesia results from chronic blockade of dopamine D2 receptors
(notably by typical antipsychotics like haloperidol). This leads to dopamine
receptor upregulation and supersensitivity, causing involuntary, repetitive
movements
Mechanism of Antipsychotics cause breast discharge By blocking D2 receptors in the tuberoinfundibular pathway, antipsychotics
reduce dopamine's inhibitory effect on prolactin secretion, causing
hyperprolactinemia and subsequent breast discharge (galactorrhea)
Antipsychotic metabolic monitoring/labs fasting blood glucose, lipid profile, weight/BMI, waist circumference, and blood
pressure. Additional labs such as liver enzymes and prolactin levels (especially
with risperidone)
treatments for bipolar depression quetiapine and lurasidone. Quetiapine acts as a dopamine and serotonin receptor
modulator, while lurasidone primarily antagonizes 5HT2A receptors with partial
D2 activity, contributing to mood stabilization
augmenting SSRIs/SNRIs in unipolar depression atypical antipsychotics like aripiprazole and brexpiprazole, and agents such as
bupropion, which enhance dopamine and norepinephrine transmission to improve
treatment response
Antipsychotic weight gain risk Clozapine highest risk, chlorpromazine mild/moderate
Antipsychotic sedation risks Highest - Clozapine, quetiapine
Moderate - olanzapine
Minimal - risperidone, aripiprazole, ziprasidone
Antispsychotic breast discharge risks Risperidone
Answers
Classic synaptic neurotransmission Action potential traveling down the presynaptic axon. Upon reaching the terminal
Ca²⁺ enters through voltage-sensitive calcium channels, triggering the exocytosis
of neurotransmitter-filled vesicles into the synaptic cleft. The released
neurotransmitters (e.g., dopamine, serotonin, norepinephrine) then bind to
postsynaptic receptors, initiating a new electrical signal in the receiving neuron.
Ligand-gated ion channel open upon neurotransmitter binding to allow rapid ion passage
Voltage-sensitive ion channel open in response to electrical changes to propagate action potentials.
Sodium-charged ion channel type of voltage-sensitive channel essential for depolarization
Presynaptic transporter (DAT, SERT, NET) clear neurotransmitters from the cleft to end the signal
Norepinephrine (NE) Regulates attention and arousal; low levels may result in ADHD/depression, while
high levels can lead to anxiety
Acetylcholine Crucial for memory and learning; deficiency is linked to Alzheimer's disease,
whereas excess may cause muscle cramps/seizures
Melatonin Synthesized in the pineal gland during darkness, it regulates the circadian rhythm
and promotes sleep
, Serotonin Modulates mood and appetite; its deficiency can cause depression/anxiety, and
excess may trigger serotonin syndrome
Dopamine Key for reward and motor control; deficiency is associated with Parkinson's and
depression, while excess is linked to schizophrenia
GABA Provides inhibitory control to prevent neuronal overexcitation; low levels may
lead to anxiety and seizures, high levels to sedation
Histamine Maintains wakefulness; overactivity can cause insomnia, and blockade (by some
antipsychotics) results in sedation and weight gain
Process of melatonin production During darkness, the pineal gland synthesizes melatonin from serotonin using N-
acetyltransferase. Melatonin levels rise at night, signaling sleep onset by acting on
MT1/MT2 receptors to regulate the circadian rhythm
Causes Tardive Dyskinesia with an antipsychotic Tardive dyskinesia results from chronic blockade of dopamine D2 receptors
(notably by typical antipsychotics like haloperidol). This leads to dopamine
receptor upregulation and supersensitivity, causing involuntary, repetitive
movements
Mechanism of Antipsychotics cause breast discharge By blocking D2 receptors in the tuberoinfundibular pathway, antipsychotics
reduce dopamine's inhibitory effect on prolactin secretion, causing
hyperprolactinemia and subsequent breast discharge (galactorrhea)
Antipsychotic metabolic monitoring/labs fasting blood glucose, lipid profile, weight/BMI, waist circumference, and blood
pressure. Additional labs such as liver enzymes and prolactin levels (especially
with risperidone)
treatments for bipolar depression quetiapine and lurasidone. Quetiapine acts as a dopamine and serotonin receptor
modulator, while lurasidone primarily antagonizes 5HT2A receptors with partial
D2 activity, contributing to mood stabilization
augmenting SSRIs/SNRIs in unipolar depression atypical antipsychotics like aripiprazole and brexpiprazole, and agents such as
bupropion, which enhance dopamine and norepinephrine transmission to improve
treatment response
Antipsychotic weight gain risk Clozapine highest risk, chlorpromazine mild/moderate
Antipsychotic sedation risks Highest - Clozapine, quetiapine
Moderate - olanzapine
Minimal - risperidone, aripiprazole, ziprasidone
Antispsychotic breast discharge risks Risperidone
